Research Paper Volume 11, Issue 11 pp 3716—3730

Long non-coding RNA MEG3 promotes fibrosis and inflammatory response in diabetic nephropathy via miR-181a/Egr-1/TLR4 axis

Figure 4. MEG3 sponging with miR-181a via direct targeting and an Ago2-dependent manner. (AD) Direct binding sites between MEG3 and miR-181a (A and C). Luciferase reporter assay was performed for the confirmation of direct binding relationship between MEG3 and miR-181a with luciferase reporter plasmids of wild- and mutant-type MEG3 (B and D). (EF) QRT-PCR demonstrated that the overexpression and silencing of MEG3 respectively decreased and increased the expression level of miR-181a; (GH) RIP assay was performed using input from cell lysate, IgG, or anti-Ago2. The relative expression levels of MEG3 and miR-181a were detected by qPCR.